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glycyrrhetinic acid (licorice) as an anticonvulsant


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Glycyrrhizic acid (from licorice) is a gap junction blocker should be an effective AC. Hence I would wager that it may be effective for BD.

I must admit this reasoning is a bit far fetched. Any particular research to support it? How gap junction blockade is related to anticonvulsant function? Also, how does it relate to bipolar disorder, given not all anticonvulsants are mood stabilizers?

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Glycyrrhizic acid (from licorice) is a gap junction blocker should be an effective AC. Hence I would wager that it may be effective for BD.

Any particular research to support it? How gap junction blockade is related to anticonvulsant function? Also, how does it relate to bipolar disorder, given not all anticonvulsants are mood stabilizers?

Glycyrrhizic acid (also as glycyrrhetinic acid)................

You might have to search PubMed separately for glycyrrhetinic acid to see its role as a gap junction blocker and then a separate search for the role for gap junction oscillations in promoting excitability and seizures.

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

The synchronized discharges typical of seizures have a multifactorial origin at molecular, cellular and network levels. During recent years, the functional role of gap-junctional coupling has received increased attention as a mechanism that may participate in seizure generation...................................

......................Initially, the effects on synaptic transmission of the gap-junctional blockers used in this study were determined. Neither carbenoxolone (CBX) nor 18-alpha-glycyrrhetinic acid altered chemical synaptic transmission at the concentrations tested. These two compounds, when injected via cannulae into the reticular nucleus of the thalamus (NRT), decreased significantly the duration of seizures as compared with saline injections or injections of the CBX inactive derivative glycyrrhizic acid. CBX injections into the hippocampus resulted in diminished seizure activity as well. NRT injections of trimethylamine, which presumably causes intracellular alkalinization (thereby promoting gap-junctional opening), enhanced seizures and spindle activity. These observations suggest that, in this rodent model, thalamic and limbic areas are involved in the synchronous paroxysmal activity and that GJC contributes to the spike-and-wave discharges.

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